Evidence map›Paper›PMID 16251443›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005

Identification of nicotinic acetylcholine receptor recycling and its role in maintaining receptor density at the neuromuscular junction in vivo.

Emile Bruneau, David Sutter, Richard I Hume, Mohammed Akaaboune

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.4field-weighted citation impact, top 12% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

67 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
  2. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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7 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Emile BruneauDepartment of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, Michigan 48109, USA.
David Sutter
Richard I Hume
Mohammed Akaaboune
Institut thématique Génétique, génomique et bioinformatique · FRUniversity of Michigan–Ann Arbor · US

Funding

The Dynamics of Synaptic Component at the Neuromuscular Junction of Living AnimalR01NS047332 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI AKAABOUNE, MOHAMMED · 2003 to 2013
$2.7M
RESEARCH TRAINING-BIOLOGICAL SCIENCEST32MH014279 · NIMH · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI AKIL, HUDA · 1986 to 2010
$1.3M
NIMH NIH HHS MH14279NIMH NIH HHS T32 MH014279NINDS NIH HHS NS047332NINDS NIH HHS R01 NS047332
6 · The paper itself

Abstract

In the CNS, receptor recycling is critical for synaptic plasticity; however, the recycling of receptors has never been observed at peripheral synapses. Using a novel imaging technique, we show here that nicotinic acetylcholine receptors (AChRs) recycle into the postsynaptic membrane of the neuromuscular junction. By sequentially labeling AChRs with biotin-bungarotoxin and streptavidin-fluorophore conjugates, we were able to distinguish recycled, preexisting, and new receptor pools at synapses in living mice. Time-lapse imaging revealed that recycled AChRs were incorporated into the synapse within hours of initial labeling, and their numbers increased with time. At fully functional synapses, AChR recycling was robust and comparable in magnitude with the insertion of newly synthesized receptors, whereas chronic synaptic activity blockade nearly abolished receptor recycling. Finally, using the same sequential labeling method, we found that acetylcholinesterase, another synaptic component, does not recycle. These results identify an activity-dependent AChR-recycling mechanism that enables the regulation of receptor density, which could lead to rapid alterations in synaptic efficacy.

Indexed as

AnimalsBiotinBungarotoxinsDiagnostic ImagingFemaleFluorescent DyesMiceNeuromuscular JunctionReceptor AggregationReceptors, NicotinicStreptavidinSynapsesTime FactorsBiotinBungarotoxinsFluorescent DyesReceptors, NicotinicStreptavidin

Identifiers

PMID16251443
PMCPMC6725561
OpenAlexW2033763111

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.